ArticleNeurochemical research2021
The Effects of Incensole Acetate on Neuro-inflammation, Brain-Derived Neurotrophic Factor and Memory Impairment Induced by Lipopolysaccharide in Rats.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Translational potential of medicinal plants for Alzheimer's disease: integrated evidence from molecular mechanisms to preclinical and clinical findings.Natural products and bioprospecting · 2026Review
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- Folic acid improved memory and learning function in a rat model of neuroinflammation induced by lipopolysaccharide.Inflammopharmacology · 2024Article
- Article
- Synthesis, characterization and anti-breast cancer potential of an incensole acetate nanoemulsion fromRSC advances · 2023Article
- BDNF-induced phrenic motor facilitation shifts from PKCθ to ERK dependence with mild systemic inflammation.Journal of neurophysiology · 2023Article
- Neuroprotective and anti-neuroinflammatory activity of frankincense in bile duct ligaion-induced hepatic encephalopathy.Iranian journal of basic medical sciences · 2023Article
- Electroacupuncture Alleviates Neuroinflammation by Inhibiting the HMGB1 Signaling Pathway in Rats with Sepsis-Associated Encephalopathy.Brain sciences · 2022Article
- Analysis of Influencing Factors of Serum Stress Index and Prognosis of HICH Patients by Different Anesthesia Methods Combined with Small Bone Window Microsurgery.Journal of healthcare engineering · 2022Article
- Acetyl-11-Keto-Evidence-based complementary and alternative medicine : eCAM · 2022Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Incensole acetate (IA) is a major component of Boswellia serrata resin that has been shown to have anti-inflammatory, anti-oxidant and neuroprotective properties. The present study determined the effect of IA on lipopolysaccharide (LPS)-induced memory impairment, and hippocampal cytokines and oxidative stress indicators level. We used 32 Wistar rats (220-250 g weight) randomly divided into four groups. The control group, which only received the saline-diluted DMSO (vehicle); LPS group which received LPS and was treated with the vehicle; and two IA-treated groups which received 2.5 or 5 mg/ kg IA before LPS injection. Morris water maze (MWM) and passive avoidance (PA) tests were performed. Finally, the brains were removed and were used to assess cytokines levels and oxidative stress status. Compared to the LPS group, IA administration reduced the time spent and path traveled to reach the hidden platform during 5 days of learning in MWM while increased the time spent in the target quadrant in the probe test. Moreover, IA increased latency while decreased entry number and time spent in the dark chamber of PA test compared to the LPS group. Additionally, pre-treatment with IA attenuated interleukin(IL)-6, tumor necrosis alpha (TNF-α), glial fibrillary acidic protein (GFAP), malondialdehyde (MDA) and nitric oxide (NO) metabolites levels while increased those of IL-10, total thiol, superoxide dismutase (SOD), catalase (CAT) and brain-derived neurotrophic factor (BDNF). Our results indicated that IA improved LPS-induced learning and memory impairments. The observed effects seem to be mediated via a protective activity against neuro-inflammation and brain tissue oxidative damage and through improving BDNF.
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